📋 Key Information Summary
- Nasal discharge character is the single most useful bedside clue: clear watery suggests allergic/viral rhinitis; thick purulent suggests acute bacterial sinusitis; unilateral bloody/foul discharge mandates urgent exclusion of foreign body or malignancy.
- Allergic rhinitis (AR) affects approximately 1 in 5 Australians and is the most common chronic nasal disorder managed in primary care; intranasal corticosteroids (INCS) are first-line pharmacotherapy.
- Acute bacterial sinusitis (ABS) should be diagnosed when symptoms persist ≥ 10 days without improvement, or worsen after initial improvement ("double sickening"); first-line antibiotic is amoxicillin 500 mg TDS for 5–7 days.
- Nasal polyps are associated with chronic rhinosinusitis, asthma, and aspirin-exacerbated respiratory disease (AERD); intranasal corticosteroids are the mainstay; biologic therapy (dupilumab) is PBS-listed for severe cases.
- Epistaxis — most bleeds originate from the anterior septum (Kiesselbach's plexus); first-aid measures (lean forward, compress soft part of nose × 10 min) control > 90% of cases.
- Recurrent or posterior epistaxis in patients on anticoagulants or with hepatic/renal disease warrants ENT referral; posterior packing carries aspiration and airway risk and should be performed in hospital.
- Hyposmia / anosmia may follow viral upper respiratory infections (including COVID-19), head trauma, or signal intracranial pathology; persistent unilateral anosmia with nasal obstruction warrants urgent imaging.
- Nasal tumours — squamous cell carcinoma is the most common sinonasal malignancy; unilateral nasal obstruction, epistaxis, facial pain, or cranial nerve palsy in an adult > 40 years should prompt urgent ENT referral (2-week wait).
- Australian-specific considerations: CA-MRSA is prevalent in remote Aboriginal and Torres Strait Islander communities and must be considered when purulent nasal/sinus infections fail initial therapy; nasal swab culture guides decolonisation regimens.
- Allergic rhinitis and asthma frequently co-exist (up to 80% of asthmatics have AR); poorly controlled AR worsens asthma outcomes — always assess both conditions together per ASCIA guidelines.
- Epistaxis in children is almost always anterior and benign; recurrent bilateral epistaxis with easy bruising warrants FBC and coagulation screen to exclude bleeding diathesis.
- MBS item 104 (specialist consultation) applies for ENT referrals; bulk-billing incentives apply for ATSI patients and those in rural/remote areas under the Practice Incentives Program (PIP).
Introduction & Australian Epidemiology
Nasal disorders encompass a broad spectrum of conditions ranging from self-limiting infectious rhinitis to life-threatening malignancies. They represent one of the most common reasons for primary care consultation in Australia, with allergic rhinitis alone accounting for an estimated 4.6 million GP encounters annually. The Australian climate — characterised by high pollen loads in temperate zones, dust in arid regions, and humidity in tropical north Queensland — creates a distinctive allergen profile that influences disease prevalence and seasonality.
The economic burden is substantial: direct healthcare costs for allergic rhinosinusitis in Australia exceed .2 billion per year when pharmacy, GP, specialist, and hospital costs are combined. Indirect costs from absenteeism and reduced workplace productivity further inflate this figure. Epistaxis accounts for approximately 1 in 200 emergency department presentations nationally, with peaks during winter (dry mucosa) and hay-fever season (mucosal inflammation).
This guideline provides an evidence-based approach to the diagnosis and management of common nasal disorders in Australian primary care and specialist practice, aligned with Therapeutic Guidelines (eTG), ASCIA, RACGP, and Australasian Society of Clinical Immunology and Allergy recommendations.
Typical Symptoms & Nasal Discharge Characteristics
A systematic approach to nasal symptoms begins with characterising the discharge (rhinorrhoea), as colour, consistency, laterality, and associated features narrow the differential diagnosis rapidly.
Discharge Character — Clinical Correlation
| Discharge Type | Appearance | Likely Diagnosis | Key Features |
|---|---|---|---|
| Clear, watery | Thin, copious, bilateral | Allergic rhinitis; viral rhinitis; CSF leak | Allergic: sneezing, itch, conjunctivitis. CSF: unilateral, post-trauma, "halo sign" |
| Mucoid (white/grey) | Thick, tenacious | Chronic rhinosinusitis; vasomotor rhinitis | Post-nasal drip, hyposmia, facial pressure |
| Mucopurulent (yellow/green) | Thick, coloured, bilateral or unilateral | Acute bacterial sinusitis; adenoiditis (children) | ≥ 10 days of symptoms or worsening after initial improvement |
| Purulent (frank pus) | Yellow-green, foul smell possible | Chronic sinusitis with nasal polyps; dental abscess eroding into maxillary sinus | Unilateral foul: dental origin or foreign body (children) |
| Bloody (epistaxis) | Bright red or dark clots | Epistaxis; nasal tumour; granulomatous disease | Unilateral recurrent: suspect structural/mass lesion |
| CSF rhinorrhoea | Clear, salty taste, unilateral | Skull base defect (trauma, surgery, spontaneous) | Positive "halo sign" on filter paper; β-2 transferrin assay confirms |
Associated Symptoms
- Nasal obstruction: Mucosal oedema (allergic, infectious), structural (deviated septum, turbinate hypertrophy), mass (polyps, tumour)
- Sneezing: Allergic rhinitis (morning predominance), viral rhinitis (first 1–2 days), vasomotor rhinitis (irritant triggers)
- Facial pain/pressure: Sinusitis (maxillary — cheek/tooth; frontal — forehead; ethmoid — between eyes; sphenoid — occipital/retro-orbital)
- Hyposmia/anosmia: CRS with polyps, post-viral (including SARS-CoV-2), head trauma, neurodegenerative disease
- Post-nasal drip: Allergic rhinitis, CRS, vasomotor rhinitis — contributes to chronic cough
Allergic Rhinitis & Sinusitis
Allergic Rhinitis (AR)
Allergic rhinitis is an IgE-mediated inflammatory disorder of the nasal mucosa triggered by aeroallergens. In Australia, the most prevalent allergens are ryegrass pollen (temperate regions), house dust mites (Dermatophagoides pteronyssinus and D. farinae), moulds (Alternaria, Cladosporium), and pet dander. AR is classified by the ARIA (Allergic Rhinitis and its Impact on Asthma) framework:
Diagnostic Approach
- Clinical diagnosis supported by characteristic history (sneezing, rhinorrhoea, nasal itch, obstruction) and typical allergen exposure pattern
- Skin prick testing (SPT) or serum-specific IgE (RAST) to confirm allergen sensitisation — available through allergists and some GP practices with allergy training
- Anterior rhinoscopy: pale, oedematous turbinates with thin clear secretions
- Nasal endoscopy (ENT): if polyps suspected, atypical features, or refractory symptoms
Pharmacological Management — Stepwise Approach
Allergen Immunotherapy
Sublingual immunotherapy (SLIT) or subcutaneous immunotherapy (SCIT) should be considered when pharmacotherapy provides inadequate symptom control or when there is a clear allergen trigger confirmed on SPT/RAST. Australian programs typically target ryegrass, house dust mite, or Alternaria. Referral to a clinical immunologist/allergist is required. MBS item 106 applies.
Sinusitis
Acute Rhinosinusitis (ARS)
Most episodes of acute rhinosinusitis are viral (common cold) and self-limiting (7–10 days). Acute bacterial sinusitis (ABS) complicates 0.5–2% of viral upper respiratory infections.
Diagnostic Criteria for ABS (IDSA 2012 / eTG)
Antibiotic Therapy for ABS
Adjunctive Measures for Sinusitis
- Intranasal saline irrigation (0.9% or hypertonic): evidence supports improved symptom clearance; available OTC (FESS®, Flo Sinus Care®)
- Intranasal corticosteroids: Fluticasone or mometasone nasal spray — reduces mucosal oedema, particularly in AR-associated sinusitis
- Short-course oral corticosteroids: Prednisolone 25–50 mg daily for 5–7 days may be considered in severe CRSwNP or when polyps cause significant obstruction
- Oral decongestants (pseudoephedrine): Short-term use (≤ 5 days) for severe congestion; contraindicated in hypertension, cardiovascular disease, and within 14 days of MAOIs
Chronic Rhinosinusitis (CRS)
CRS is defined as symptomatic sinus inflammation lasting ≥ 12 weeks. It is subdivided into CRS without nasal polyps (CRSsNP) and CRS with nasal polyps (CRSwNP). Australian prevalence is approximately 10–12%. Diagnosis requires ≥ 2 of: nasal obstruction, anterior/posterior rhinorrhoea, facial pressure/pain, hyposmia/anosmia, plus either endoscopic or CT evidence of inflammation. Management involves prolonged INCS, saline irrigation, and ENT referral for endoscopic sinus surgery (ESS) if medical therapy fails after ≥ 3 months.
Nasal Polyps & Epistaxis
Nasal Polyps
Nasal polyps are benign, oedematous, semi-translucent grape-like projections arising from the paranasal sinus mucosa, most commonly from the ethmoid sinuses. They affect 1–4% of the adult population and are rare in children (consider cystic fibrosis if polyps found in a child).
Associations
- Asthma — up to 40–70% of CRSwNP patients have coexisting asthma
- Aspirin-exacerbated respiratory disease (AERD / Samter's triad): asthma + nasal polyps + NSAID/COX-1 sensitivity; present in 7–15% of asthmatic adults with polyps
- Allergic fungal rhinosinusitis — especially in atopic patients in tropical/subtropical Australia
- Cystic fibrosis — nasal polyps found in 10–40% of CF patients; bilateral
- Primary ciliary dyskinesia
Management of Nasal Polyps
Epistaxis
Epistaxis (nosebleed) is classified by location: anterior (90–95%) from Kiesselbach's plexus on the nasal septum, and posterior (5–10%) from branches of the sphenopalatine or ethmoid arteries. Posterior bleeds are more common in elderly patients, those on anticoagulants, and those with uncontrolled hypertension.
Aetiology
| Category | Common Causes |
|---|---|
| Local | Digital trauma (nose picking — most common in children), dry air/heating, allergic rhinitis, nasal septal deviation, foreign body, INCS use, nasal septal perforation, tumour |
| Systemic | Anticoagulant/antiplatelet therapy (warfarin, DOACs, aspirin, clopidogrel), liver cirrhosis/coagulopathy, thrombocytopenia, hereditary haemorrhagic telangiectasia (HHT/Osler-Weber-Rendu), hypertension (association debated but may exacerbate), vasculitis |
Stepwise Management of Epistaxis
Disorders of Smell & Nasal Tumours
Disorders of Smell (Dysosmia)
Olfactory dysfunction is broadly classified as quantitative (hyposmia — reduced; anosmia — absent; hyperosmia — enhanced) or qualitative (parosmia — distorted perception; phantosmia — olfactory hallucination). In Australia, post-viral olfactory loss (including post-COVID-19) is now the most common cause, followed by CRSwNP and post-traumatic olfactory dysfunction.
Common Aetiologies
| Mechanism | Causes | Typical Presentation |
|---|---|---|
| Conductive (transport) | Allergic rhinitis, CRS, nasal polyps, septal deviation, turbinate hypertrophy | Bilateral smell loss; improves when obstruction relieved (e.g., decongestant trial) |
| Sensorineural (epithelial) | Post-viral (SARS-CoV-2, influenza, parainfluenza), toxic exposure (smoking, industrial chemicals), medications (intranasal zinc, methotrexate) | Acute onset following URI; may recover over 6–12 months; parosmia common during recovery |
| Neural (central) | Head trauma, neurodegenerative disease (Parkinson's, Alzheimer's), intracranial tumours (olfactory groove meningioma, frontal lobe glioma), epilepsy (uncinate fits) | Gradual or sudden onset; may be unilateral; associated neurological signs |
Investigation and Management
- Bedside testing: Assess each nostril separately using coffee, peppermint, or vanilla; standardised tools include the Sniffin' Sticks test or University of Pennsylvania Smell Identification Test (UPSIT) — available through ENT and neurology clinics
- Nasal endoscopy: Evaluate for polyps, masses, or mucosal disease
- MRI brain (with gadolinium): Indicated for unilateral anosmia, suspected intracranial pathology, or post-traumatic loss with focal neurological signs
- Post-viral olfactory training: Sniff 4 essential oils (rose, eucalyptus, lemon, clove) for 20 seconds each, twice daily, for ≥ 12 weeks. Evidence supports modest improvement in olfactory scores. Free resources available through Fifth Sense (UK) and adapted by ASCIA
- Intranasal corticosteroids: May benefit conductive and some post-viral cases; high-volume sinonasal rinses with budesonide (off-label) used by ENT for CRS-related hyposmia
- Alpha-lipoic acid (600 mg PO OD): Limited evidence for post-viral anosmia; may be trialled for 3 months
Nasal Tumours
Primary sinonasal tumours are rare, accounting for < 1% of all malignancies in Australia. Benign tumours are more common than malignant. A high index of suspicion is required as early symptoms are non-specific.
Benign Tumours
| Tumour | Key Features | Management |
|---|---|---|
| Inverting papilloma | Most common benign sinonasal tumour. Unilateral nasal obstruction, arises from lateral nasal wall. 5–15% malignant transformation to SCC. | Complete surgical excision (wide local excision via ESS). Long-term endoscopic follow-up essential. |
| Haemangioma | Red/blue mass on septum (capillary) or lateral wall (venous/cavernous). Recurrent epistaxis. | Surgical excision or laser ablation. |
| Ossifying fibroma | Slow-growing bony tumour of the mandible or maxilla; may extend into sinuses. | Surgical excision. |
| Juvenile nasopharyngeal angiofibroma (JNA) | Highly vascular tumour in adolescent males. Unilateral nasal obstruction + recurrent profuse epistaxis. CT/MRI shows characteristic bowing of posterior maxillary wall. | Pre-operative angioembolisation + surgical resection. Refer to paediatric ENT or skull-base centre. |
Malignant Tumours
| Tumour | Prevalence | Key Features | Management |
|---|---|---|---|
| Squamous cell carcinoma (SCC) | Most common sinonasal malignancy (~50–60%) | Unilateral nasal obstruction, epistaxis, facial pain, cheek swelling. Associated with hardwood dust (occupational), nickel, leather dust. | Surgery + adjuvant radiotherapy. MDT at tertiary centre. |
| Adenoid cystic carcinoma | 10–15% of sinonasal malignancies | Slow-growing; perineural invasion (V2, V3) is hallmark. Late recurrence (10–20 years). | Surgery + radiotherapy. Lifelong surveillance. |
| Esthesioneuroblastoma (olfactory neuroblastoma) | Rare (~3–5%) | Arises from olfactory epithelium at skull base. Unilateral nasal obstruction, epistaxis, anosmia. Bimodal age distribution (young adults + 50–60 years). | Craniofacial resection + radiotherapy ± chemotherapy. Kadish staging. |
| Mucosal melanoma | Rare (~3–5%) | Darkly pigmented (or amelanotic) mass. Aggressive with early metastasis. | Surgery + immunotherapy (checkpoint inhibitors). Refer melanoma MDT. |
| Non-Hodgkin lymphoma (NHL) | ~5–10% | NK/T-cell lymphoma (nasal-type) — more common in Asian/Indigenous Australian populations. Midline destructive lesion, "lethal midline granuloma". | Chemoradiotherapy. Refer haematology MDT. |
Staging and Imaging
- CT sinuses (non-contrast): First-line for suspected structural/mass lesion; demonstrates bony erosion, involvement of orbit/skull base
- MRI with gadolinium: Superior for soft-tissue characterisation, intracranial extension, perineural spread, and orbital involvement. Essential for staging
- PET-CT: For staging of malignant sinonasal tumours; assesses regional and distant metastases
- Biopsy: Must be performed under ENT guidance (endoscopic); avoid blind biopsy due to risk of bleeding and incomplete sampling. JNA is typically not biopsied (imaging diagnosis) due to haemorrhage risk.
Investigations
Investigations for nasal disorders should be guided by clinical context. The majority of acute presentations (viral rhinitis, simple anterior epistaxis) require no laboratory or imaging workup.
Empirical Therapy
Empirical treatment decisions are guided by clinical presentation and likelihood of aetiology. Most acute nasal complaints are managed symptomatically before diagnostic confirmation.
Monitoring
- Allergic rhinitis: Review at 4–8 weeks after initiating INCS; assess symptom control (ARIA classification), nasal obstruction severity, impact on sleep/work/asthma. Step down if well controlled; step up (add antihistamine, combination spray, or refer for immunotherapy) if persistent.
- Acute bacterial sinusitis: Review at 48–72 hours if no improvement or worsening; consider alternative antibiotic or imaging. Repeat review at 7 days to confirm resolution.
- Chronic rhinosinusitis: Assess at 3-monthly intervals using validated symptom scores (SNOT-22). CT at baseline and post-operatively. Monitor for polyp recurrence after ESS.
- Nasal polyps on dupilumab: Monitor at 16 weeks (first assessment point), then 6-monthly. Assess SNOT-22, NPS (Nasal Polyp Score), olfaction, asthma control (if concurrent), and eosinophil count.
- Recurrent epistaxis: Monitor haemoglobin if frequent bleeds. Review anticoagulant appropriateness. Screen for hereditary haemorrhagic telangiectasia (HHT) if recurrent nosebleeds with telangiectasia and family history (Curacao criteria).
- Post-surgical (ESS): Endoscopic surveillance at 2 weeks, 6 weeks, 3 months, 6 months, and 12 months post-surgery, then annually if CRSwNP. Ongoing INCS is mandatory.
- Sinonasal malignancy post-treatment: Clinical examination + nasal endoscopy every 3 months for 2 years, then every 6 months for 3 years, then annually. CT/MRI per oncology protocol.
Special Populations
Aboriginal and Torres Strait Islander Health
Nasal and sinus disease disproportionately affects Aboriginal and Torres Strait Islander Australians, particularly those living in remote and very remote communities. Otitis media with effusion (OME) and upper respiratory tract infections are among the most common childhood conditions, and chronic rhinosinusitis in adults is frequently complicated by CA-MRSA colonisation and recurrent antibiotic-resistant infections.
📚 References
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